Knowledge, attitude, practice and perception on sunscreen and skin cancer among doctors and pharmacists.

INTRODUCTION: Excessive ultraviolet light (UV) can cause premature skin aging and potentially skin cancer. Currently there is a lack of awareness among health care professionals and the public on sun protection. The objectives of this study were to determine knowledge on sunscreen and skin cancer among health care professionals, to evaluate the knowledge, attitude, practice and perception of doctors and pharmacists toward the usage of sunscreen as protection against UV radiation. MATERIALS AND METHODS: This is a cross-sectional study conducted among doctors and pharmacists in Hospital Sultanah Nora Ismail, Batu Pahat, Johor, Malaysia. Questionnaires were used in this study. RESULTS: A total of 384 participants completed the questionnaires. The participants consisted of 323 doctors (84.1%) and 61 pharmacists (15.9%). The age group of the participants ranged between 25 till 55 years old. Ninety doctors (27.9%) and thirty-one pharmacists (51.0%) reported used sunscreen daily (p<0.001). This finding showed that there was a deficit in the practice of sun protection. Pharmacists scored a higher knowledge score of median 12 (IQR=3.0) while the doctors scored 11 (IQR=2.0). This study showed a significant association between ethnicity and skin cancer knowledge (p<0.05). CONCLUSION: This study demonstrated a lack of knowledge of sunscreen and skin cancer prevention among health care practitioners. This finding supports better medical education program on this topic.

Not all swellings are lymph nodes! A case of subcutaneous panniculitis-like T-cell lymphoma.

Subcutaneous Panniculitis-like T-cell Lymphoma (SPTL) is a rare cutaneous neoplasm of mature cytotoxic T cells, first described in 1991 by Gonzalez et al. The incidence of SPTL in Asian countries ranges from 2.3% to 3%. In Malaysia, only 5 cases were reported from 2001 to 2004 in Hospital Kuala Lumpur, Malaysia. SPTL typically presents as skincoloured or erythematous subcutaneous nodules, most often on the extremities and trunk, but it can also involve the face, back and neck. Diagnosis of SPTL is made based on correlation of clinical findings and subcutaneous tissue biopsy along with immunohistochemical staining patterns.

Effects of finishing/polishing techniques on microleakage of resin-modified glass ilonomer cement restorations.

This study investigated the effect of finishing/polishing techniques on the microleakage of resin-modified glass ionomer restorations. Class V preparations were made on the buccal and lingual/palatal surfaces of freshly extracted teeth. The cavities on each tooth were restored with Fuji II LC (FT [GC]) and Photac-Fil Quick (PF [3M-ESPE]) according to manufacturers' instructions. Immediately after light-polymerization, gross finishing was done with eight-fluted tungsten carbide burs. The teeth were then randomly divided into four groups and finishing/polishing was done with one of the following systems: (a) Robot Carbides (RC); (b) Super-Snap system (SS); (c) OneGloss (OG) and (d) CompoSite Polishers (CS). The sample size for each material-finishing/polishing system combination was eight. After finishing/polishing, the teeth were stored in distilled water at 37 degrees C for one week. The root apices were then sealed with acrylic and two coats of varnish was applied 1 mm beyond the restoration margins. The teeth were subsequently subjected to dye penetration testing (0.5% basic fuchsin), sectioned and scored. Data was analyzed using Kruskal-Wallis and Mann-Whitney U tests at a significance level of 0.05. Results of statistical analysis were as follows: Enamel margins: PF-OG

Effects of instrumentation time on microleakage of resin-modified glass ionomer cements.

This study investigated the effect of instrumentation time on the microleakage of resin-modified glass ionomer cements (RMGICs). Class V cavities were prepared on buccal and lingual/ palatal surfaces of 64 freshly extracted non-carious premolars. The cavities on each tooth were restored with Fuji II LC (FT [GC]) and Photac-Fil Quick (PF [3M-ESPE]). The restored teeth were randomly divided into two groups of 32 teeth. Finishing/polishing was done immediately after light-polymerization in one group and was delayed for one week in the other group. The following finishing/polishing systems were evaluated: (a) Robot Carbides (RC); (b) SuperSnap (SS); (c) OneGloss (OG) and (d) CompoSite Polishers (CS). The sample size for each instrumentation time, material and finishing/polishing system combination was 8. Storage medium for both immediate and delayed instrumentation groups was distilled water at 37 degrees C during the hiatus period. The teeth were subsequently subjected to dye penetration testing (0.5% basic fushcin), sectioned and scored. Data were analyzed using Kruskal-Wallis and Mann-Whitney U tests at significance level 0.05. For PF, significant difference in enamel leakage was observed between immediate and delayed instrumentation with SS and CS. Significant differences in dentin leakage were also observed between the two instrumentation times for SS. For FT, significant differences in leakage between instrumentation times were observed only in dentin and with RC. Where significant differences in dye penetration scores existed, delayed finishing/polishing resulted in less microleakage.

Surface texture of resin-modified glass ionomer cements: effects of finishing/polishing time.

This study compared the surface texture of resin-modified glass ionomer cements after immediate and delayed finishing with different finishing/polishing systems. Class V preparations were made on the buccal and lingual/palatal surfaces of 64 freshly extracted teeth. The cavities on each tooth were restored with Fuji II LC (GC) and Photac-Fil Quick (3M-ESPE) according to manufacturers' instructions. Immediately after light-polymerization, gross finishing was done with 8-fluted tungsten carbide burs. The teeth were then randomly divided into four groups of 16 teeth. Half of the teeth in each group were finished immediately, while the remaining half were finished after one-week storage in distilled water at 37 degrees C. The following finishing/polishing systems were employed: (a) Robot Carbides; (b) Super-Snap system; (c) OneGloss and (d) CompoSite Polishers. The mean surface roughness (microm; n=8) in vertical (RaV) and horizontal (RaH) axis was measured using a profilometer. Data was subjected to ANOVA/Scheffe's tests and Independent Samples t-test at significance level 0.05. Ra values were generally lower in both vertical and horizontal axis with delayed finishing/polishing. Although significant differences in RaV and RaH values were observed among several systems with immediate finishing/polishing, only one (Fuji II LC: RaH - Super-Snap < Robot Carbides) was observed with delayed finishing.

Surface texture of resin-modified glass ionomer cements: effects of finishing/polishing systems.

This study investigated the surface texture of two resin-modified glass ionomer cements (RMGICs) in the vertical and horizontal axis after treatment with different finishing/polishing systems. Class V preparations were made on the buccal and lingual/palatal surfaces of freshly extracted teeth. The cavities on each tooth were restored with Fuji II LC (GC) and Photac-Fil Quick (ESPE) according to manufacturers' instructions. Immediately after light-polymerization, gross finishing was done with 8-flute tungsten carbide burs. The teeth were then randomly divided into four groups and finished/polished with (a) Robot Carbides (RC); (b) Super-Snap system (SS); (c) OneGloss (OG) and (d) CompoSite Points (CS). The sample size for each material-finishing/polishing system combination was eight. The mean surface roughness (microm) in vertical (RaV) and horizontal (RaH) axis was measured using a profilometer. Data was subjected to ANOVA/Scheffe's tests and Independent Samples t-test at significance level 0.05. Mean RaV ranged from 0.59-1.31 and 0.83-1.52, while mean RaH ranged from 0.80-1.43 and 0.85-1.58 for Fuji II LC and Photac-Fil, respectively. Results of statistical analysis were as follows: Fuji II LC: RaV-RC, SS

Human variability and susceptibility to trichloroethylene.

Although humans vary in their response to chemicals, comprehensive measures of susceptibility have generally not been incorporated into human risk assessment. The U.S. EPA dose-response-based risk assessments for cancer and the RfD/RfC (reference dose-reference concentration) approach for noncancer risk assessments are assumed to protect vulnerable human subgroups. However, these approaches generally rely on default assumptions and do not consider the specific biological basis for potential susceptibility to a given toxicant. In an effort to focus more explicitly on this issue, this article addresses biological factors that may affect human variability and susceptibility to trichloroethylene (TCE), a widely used halogenated industrial solvent. In response to Executive Order 13045, which requires federal agencies to make protection of children a high priority in implementing their policies and to take special risks to children into account when developing standards, this article examines factors that may affect risk of exposure to TCE in children. The influence of genetics, sex, altered health state, coexposure to alcohol, and enzyme induction on TCE toxicity are also examined.

Polychlorinated biphenyls and 2,3,7,8-tetrachlorodibenzo-p-dioxin induce intrachromosomal recombination in vitro and in vivo.

Polychlorinated aromatic hydrocarbons such as polychlorinated biphenyls and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) are extremely stable and widely distributed environmental pollutants. These chemicals are animal carcinogens and probable human carcinogens, and TCDD is possibly one of the most potent toxins ever evaluated by the United States Environmental Protection Agency. Polychlorinated aromatic hydrocarbons score negatively in most genotoxicity assays, including the Ames (Salmonella) assay. Although their mechanism of toxicity is not well understood, they induce aryl hydrocarbon (AH) hydroxylases and bind to the AH receptor, which is believed to mediate toxicity. Here, we determine effects of polychlorinated aromatic hydrocarbons in genotoxicity assays that score for DNA deletions by intrachromosomal recombination in vivo and in vitro. In this study, TCDD, Aroclor 1221, and Aroclor 1260 induced deletions in vivo in the mouse embryo; Aroclor 1221 and Aroclor 1260 induced deletions in yeast. We also show that the induced deletion events did not correlate with induction of AH hydroxylase. None of the tested compounds induced CYP1A-associated ethoxyresorufin-O-deethylase activity in mouse embryos or in vitro. These results clearly demonstrate a genotoxic activity of polychlorinated aromatic hydrocarbons in vitro and in vivo, which is independent of induction of cytochrome P450 activity. Because genetic instability and deletions may be mechanistically involved in carcinogenesis, these results may encourage further research to determine whether such genotoxic mechanisms may be useful for cancer risk assessment of polychlorinated aromatic hydrocarbons.

Nature of abortive transformation in Saccharomyces cerevisiae.

Disruption mutagenesis by homologous recombination in Saccharomyces cerevisiae is carried out by transforming-DNA fragments containing the target gene disrupted by a selectable marker. A large number of transient (abortive) transformants are often formed that may hinder the isolation of integrants containing the gene disruption. We show that abortive transformants result from re-circularization of the linear transforming-DNA in vivo. Their number was greatly reduced when the cut DNA could not readily re-ligate, either by digestions that gave non-compatible or blunt ends, or by de-phosphorylation. In addition, true integrants could be readily distinguished from abortive transformants through replica plating onto selective media. Enhanced disruption-mutagenesis was also observed when non-compatible ends were generated in an ARS-containing insertion vector.

Recombination hotspots in bacteriophage T4 are dependent on replication origins.

Bacteriophage T4 recombination "hotspots" were first detected by the rescue of genetic markers from UV-irradiated phage particles. These hotspots have since been detected following treatments that yield other forms of DNA damage, and at least one is active in the absence of damage. The previous mapping of phage replication origins near the peaks of two recombination hotspots suggested that the origins cause the localized enhancement of recombination. Here we show that deletion of one origin eliminates the corresponding recombination hotspot, as judged by rescue of markers from UV-irradiated phage. Furthermore, insertion of either origin into a recombination "coldspot" enhances rescue of nearby markers. We conclude that these origins are necessary, and very likely sufficient, for the generation of recombination hotspots. We also show that the hotspots are active in the absence of both phage-encoded UvsY and host-encoded RecA proteins, suggesting that some of the stimulated recombination occurs by a synaptase-independent mechanism.

Tertiary initiation of replication in bacteriophage T4. Deletion of the overlapping uvsY promoter/replication origin from the phage genome.

Tertiary initiation of bacteriophage T4 DNA replication is resistant to the RNA polymerase inhibitor rifampicin and apparently involved in the activity of recombination hot spots in the T4 genome (Kreuzer, K. N., and Alberts, B. M. (1985) Proc. Natl. Acad. Sci. U. S. A. 82, 3345-3349). One of the origins that function by the tertiary mechanism maps at the promoter for gene uvs Y. A deletion and a linker-insertion mutation in the uvsY promoter/origin region were generated by in vitro manipulations and then placed into the T4 genome using the insertion/substitution system (Selick, H. E., Kreuzer, K. N., and Alberts, B. M. (1988) J. Biol. Chem. 263, 11336-11347). Both resulting phage strains are uvsY- mutants, but they differ in that one has a deletion of the minimal tertiary origin and the other does not. The effects of the uvsY mutations on tertiary origin activity were assayed by infecting tertiary origin plasmid-bearing Escherichia coli with the two phage mutants. The tertiary origin plasmids replicated extensively after infection by either uvsY- phage mutant, demonstrating that the uvsY protein is not required for tertiary initiation. The extent of plasmid replication was increased dramatically as a result of either mutation, indicating that the uvsY protein plays some negative role in either the initiation or subsequent processing of plasmid replicative intermediates. The phage strain with an origin deletion induced the replication of a tertiary origin plasmid with which it shared no homology. Therefore, plasmid-phage recombination is not required for the replication of tertiary origin plasmids. The replication of a tertiary origin plasmid is also shown to be independent of the phage genes uvsX, 59, and 46, but markedly reduced by mutations in the T4-induced topoisomerase.

Recombination-dependent replication of plasmids during bacteriophage T4 infection.

The replication of plasmids containing fragments of the T4 genome, but no phage replication origins, was analyzed as a possible model for phage secondary (recombination-dependent) replication initiation. The replication of such plasmids after T4 infection was reduced or eliminated by mutations in several phage genes (uvsY, uvsX, 46, 59, 39, and 52) that have previously been shown to be involved in secondary initiation. A series of plasmids that collectively contain about 60 kilobase pairs of the T4 genome were tested for replication after T4 infection. With the exception of those known to contain tertiary origins, every plasmid replicated in a uvsY-dependent fashion. Thus, there is no apparent requirement for an extensive nucleotide sequence in the uvsY-dependent plasmid replication. However, homology with the phage genome is required since the plasmid vector alone did not replicate after phage infection. The products of plasmid replication included long concatemeric molecules with as many as 35 tandem copies of plasmid sequence. The production of concatemers indicates that plasmid replication is an active process and not simply the result of passive replication after the integration of plasmids into the phage genome. We conclude that plasmids with homology to the T4 genome utilize the secondary initiation mechanism of the phage. This simple model system should be useful in elucidating the molecular mechanism of recombination-dependent DNA synthesis in phage T4.

Immunosuppression in autoimmune disease: the double-edged sword.

We have developed a protocol of prophylactic cyclosporin A administration which confers complete and permanent protection against insulin-dependent diabetes mellitus in diabetes-prone BioBreeding rats. Spontaneous insulin-dependent diabetes mellitus developed in about 50% of BioBreeding rats, between 10 and 18 weeks of age. Prophylactic cyclosporin A (10 mg/kg/day p.o.), started at 6 weeks of age and terminated at 21 weeks of age, completely prevented insulin-dependent diabetes mellitus: 0% (0/25) cyclosporin A-treated compared to 46% (11/24) control rats developed insulin-dependent diabetes mellitus (p less than 0.001). Protection against insulin-dependent diabetes mellitus was lifelong, provided cyclosporin A prophylaxis was initiated when insulitis was minimal or absent, and pancreatic insulin content was normal. Cyclosporin A prophylaxis initiated later, but still before the onset of clinical symptoms (8-9 weeks), and terminated at 22-23 weeks, was only partially effective; 5/20 (25%) of cyclosporin A-treated rats developed insulin-dependent diabetes mellitus, compared to 60% (12/20) of controls (p less than 0.05). Cyclosporin A prophylaxis started at the appropriate time (6 weeks) but terminated prematurely (17-19 weeks of age) was not effective; insulin-dependent diabetes mellitus developed in 20% (3/15), compared to 50% (7/14) controls (p greater than 0.05); insulin-dependent diabetes mellitus developed after cessation of therapy. We conclude that effective and permanent moderate-dose cyclosporin A prophylaxis of insulin-dependent diabetes mellitus in BioBreeding rats requires (1) early initiation of treatment, when islet morphology and hormone content are still normal; and (2) prolonged treatment, with continuation of prophylaxis past the end of the at-risk period.(ABSTRACT TRUNCATED AT 250 WORDS)

Cyclosporin prophylaxis induces long-term prevention of diabetes, and inhibits lymphocytic infiltration in multiple target tissues in the high-risk BB rat.

Spontaneous insulin-dependent diabetes mellitus (IDDM) and other autoimmune manifestations, such as lymphocytic thyroiditis and atrophic gastritis, develop in diabetes-prone (high-risk) lines of Wistar-derived BioBreeding (BB) rats. To examine whether Cyclosporin A (CsA) would abrogate multiple autoimmune manifestations in BB rats, we treated them prophylactically with CsA from 5-6 weeks to 23-25 weeks of age. IDDM developed in 0/58 CsA-treated rats; 47% (29 out of 62) of sex- and age-matched controls treated with vehicle developed IDDM (p less than 0.001). CsA-treated rats had no or minimal lymphocytic infiltration and parenchymal changes in the pancreas, stomach and thyroid at the time of cessation of treatment. IDDM, glycosuria and hyperglycemia developed in 0/22 rats followed up to 370 days of age (up to 210 days following the cessation of CsA therapy); histologic examination of their islets was normal. We conclude that CsA completely abrogates the development of clinical IDDM in the BB rat, and that it inhibits or abolishes lymphocyte infiltration in several organs against which there is autoimmunity. The data also suggest that the protective effect of CsA persists well past the duration of therapy, and that cell-mediated autoimmunity (with or without humoral immunity) may be an important pathogenetic mechanism in the destruction of beta cells in the BB rat.